The flare reaction in allergic contact dermatitis is an activation (inflammation) of old ACD challenge sites when the allergen is given parenterally. We have evidence that this is a T cell reaction, or at least that B cells or B cell products are not required. We shall characterize the histology, kinetics and lability of the flare reaction utilizing models that we have developed in the mouse and rat. Methods for modulating the intensity of induced ACD will be explored giving particular attention to cyclophosphamide, C.parvum (P.acnes)and haptenized lymphoid cells. The parameters leading to immunopotentiation by cyclophosphamide in the human will be worked out and mechanisms examined. Mice can be rendered B cell deficient by chronic treatment, beginning within first 24 hours of birth, with heterologous anti-sera directed against mouse IgM. This B cell deficient mouse model we shall continue to exploit so as to determine the contribution of B cells, and B cell factors, in the regulation and expression of allergic contact dermatitis.